Jennifer Mancio1, Antonio S Barros2, Gloria Conceicao2, Guilherme Pessoa-Amorim2, Catia Santa3, Carla Bartosch4, Wilson Ferreira5, Monica Carvalho5, Nuno Ferreira5, Luis Vouga6, Isabel M Miranda2, Rui Vitorino2, Bruno Manadas7, Ines Falcao-Pires2, Vasco Gama Ribeiro5, Adelino Leite-Moreira8, Nuno Bettencourt2. 1. Department of Surgery and Physiology, Cardiovascular Research Unit (UnIC), Faculty of Medicine, University of Porto, Portugal; Department of Cardiology, Centro Hospitalar de Vila Nova de Gaia, Portugal. Electronic address: up200104593@med.up.pt. 2. Department of Surgery and Physiology, Cardiovascular Research Unit (UnIC), Faculty of Medicine, University of Porto, Portugal. 3. CNC - Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal; III: Institute for Interdisciplinary Research, University of Coimbra (IIIUC), Portugal. 4. Department of Pathology, Portuguese Oncology Institute of Porto, Porto, Portugal. 5. Department of Cardiology, Centro Hospitalar de Vila Nova de Gaia, Portugal. 6. Department of Cardiothoracic Surgery, Centro Hospitalar de Vila Nova de Gaia, Portugal. 7. CNC - Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal. 8. Department of Surgery and Physiology, Cardiovascular Research Unit (UnIC), Faculty of Medicine, University of Porto, Portugal; Department of Cardiothoracic Surgery, Centro Hospitalar de Sao Joao, Portugal.
Abstract
BACKGROUND & AIMS: The role of epicardial adipose tissue (EAT) in the pathophysiology of late stage-coronary artery disease (CAD) has not been investigated. We explored the association of EAT volume and its proteome with advanced coronary atherosclerosis. METHODS: The EPICHEART Study prospectively enrolled 574 severe aortic stenosis patients referred to cardiac surgery. Before surgery, EAT volume was quantified by computed tomography (CT). During surgery, epicardial, mediastinal (MAT) and subcutaneous (SAT) adipose tissue samples were collected to explore fat phenotype by analyzing the proteomic profile using SWATH-mass spectrometry; pericardial fluid and peripheral venous blood were also collected. CAD presence was defined as coronary artery stenosis ≥50% in invasive angiography and by CT-derived Agatston coronary calcium score (CCS). RESULTS: EAT volume adjusted for body fat was associated with higher CCS, but not with the presence of coronary stenosis. In comparison with mediastinal and subcutaneous fat depots, EAT exhibited a pro-calcifying proteomic profile in patients with CAD characterized by upregulation of annexin-A2 and downregulation of fetuin-A; annexin-A2 protein levels in EAT samples were also positively correlated with CCS. We confirmed that the annexin-A2 gene was overexpressed in EAT samples of CAD patients and positively correlated with CCS. Fetuin-A gene was not detected in EAT samples, but systemic fetuin-A was higher in CAD than in non-CAD patients, suggesting that fetuin-A was locally downregulated. CONCLUSIONS: In an elderly cohort of stable patients, CCS was associated with EAT volume and annexin-A2/fetuin-A signaling, suggesting that EAT might orchestrate pro-calcifying conditions in the late phases of CAD.
BACKGROUND & AIMS: The role of epicardial adipose tissue (EAT) in the pathophysiology of late stage-coronary artery disease (CAD) has not been investigated. We explored the association of EAT volume and its proteome with advanced coronary atherosclerosis. METHODS: The EPICHEART Study prospectively enrolled 574 severe aortic stenosispatients referred to cardiac surgery. Before surgery, EAT volume was quantified by computed tomography (CT). During surgery, epicardial, mediastinal (MAT) and subcutaneous (SAT) adipose tissue samples were collected to explore fat phenotype by analyzing the proteomic profile using SWATH-mass spectrometry; pericardial fluid and peripheral venous blood were also collected. CAD presence was defined as coronary artery stenosis ≥50% in invasive angiography and by CT-derived Agatston coronary calcium score (CCS). RESULTS: EAT volume adjusted for body fat was associated with higher CCS, but not with the presence of coronary stenosis. In comparison with mediastinal and subcutaneous fat depots, EAT exhibited a pro-calcifying proteomic profile in patients with CAD characterized by upregulation of annexin-A2 and downregulation of fetuin-A; annexin-A2 protein levels in EAT samples were also positively correlated with CCS. We confirmed that the annexin-A2 gene was overexpressed in EAT samples of CAD patients and positively correlated with CCS. Fetuin-A gene was not detected in EAT samples, but systemic fetuin-A was higher in CAD than in non-CAD patients, suggesting that fetuin-A was locally downregulated. CONCLUSIONS: In an elderly cohort of stable patients, CCS was associated with EAT volume and annexin-A2/fetuin-A signaling, suggesting that EAT might orchestrate pro-calcifying conditions in the late phases of CAD.
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